The aim of the proposed research is to determine the effects of oxytocin (OT) on the phosphorylation, and hence activity, of the transcription regulator cyclic adenosine monophosphate (cAMP) response element binding (CREB) protein in the medial amygdala (MeA), and the effect on social attachment. CREB activation underlies many forms of synaptic plasticity, including learning, memory, and addiction. Social attachment is another critical form of behavioral plasticity, and the proposed research will examine whether OT also influences CREB activity. There is a large body of literature supporting a role for OT in the attachment process, and while many areas of the brain are implicated, the discrete signaling mechanisms invovled remain to be elucidated. Additionally, given the similarities between attachment and addictive processes, social attachment can be used to determine the molecular bases of addiction and the responses to withdrawal. This study will focus on the effects of OT in the MeA. This nucleus is one of the first parts of the brain to respond to social stimuli, and drugs of abuse lead to alterations in signaling within the MeA. Therefore, the physiological and behavioral adaptations that occur during drug use and withdrawal (reduced CREB activity) may be attenuated by OT in the MeA. OT is expected to increase CREB phosphorylation in the MeA and thereby facilitate social attachment. I will test this hypothesis using prairie voles (Microtus ochrogaster) as a model, as the social system of prairie voles closely resembles that of humans.